Our working hypothesis is that there are at least four different forms of hypertriglyceridemia: (1) mutations in the lipoprotein lipase (LPL) gene; (2) overproduction of apoB and triglycerides (TG), familial combined hyperlipidemia; (3) overproduction of TG and normal apoB production, type IV primary hypertriglyceridemia; and (4) overproduction of apoC-III, mutation in the apo AI-CIII-AIV gene cluster. These different forms can be defined by metabolic studies designed to assess the in vivo production rate of these components. As the first phase, the present proposal will develop an efficient protocol based on non-radioactive tracers which can allow the production of apoB, apoE, apoC-III and TG to be determined simultaneously in humans.